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Cadmium (Cd) and excess molybdenum (Mo) are multiorgan toxic, but the detrimental impacts of Cd and/or Mo on poultry have not been fully clarified. Thence, a 16‐week sub‐chronic toxic experiment was executed with ducks to assess the toxicity of Cd and/or Mo. Our data substantiated that Cd and Mo coexposure evidently reduced GSH‐Px, GSH, T‐SOD, and CAT activities and elevated H2O2 and MDA concentrations in myocardium. What is more, the study suggested that Cd and Mo united exposure synergistically elevated Fe2+ content in myocardium and activated AMPK/mTOR axis, then induced ferroptosis by obviously upregulating ACSL4, PTGS2, and TFRC expression levels and downregulating SLC7A11, GPX4, FPN1, FTL1, and FTH1 expression levels. Additionally, Cd and Mo coexposure further caused excessive ferritinophagy by observably increasing autophagosomes, the colocalization of endogenous FTH1 and LC3, ATG5, ATG7, LC3II/LC3I, NCOA4, and FTH1 expression levels. In brief, this study for the first time substantiated that Cd and Mo united exposure synergistically induced ferroptosis and excess ferritinophagy by AMPK/mTOR axis, finally augmenting myocardium injure in ducks, which will offer an additional view on united toxicity between two heavy metals on poultry. [ABSTRACT FROM AUTHOR]

Excess molybdenum (Mo) is harmful to animals, but its nephrotoxicity has not been comprehensively explained. To appraise the influences of excess Mo on Ca homeostasis and apoptosis via PLC/IP3/IP3R axis, primary duck renal tubular epithelial cells were exposed to 480 μM and 960 μM Mo, and joint of 960 μM Mo and 10 μM 2‐APB or 0.125 μM U‐73122 for 12 h (U‐73122 pretreated for 1 h), respectively. The data revealed that the increment of [Ca2+]c induced by Mo mainly originated from intracellular Ca storage. Mo exposure reduced [Ca2+]ER, elevated [Ca2+]mit, [Ca2+]c, and the expression of Ca homeostasis‐related factors (Calpain, CaN, CRT, GRP94, GRP78 and CaMKII). 2‐APB could effectively reverse subcellular Ca2+ redistribution by inhibiting IP3R, which confirmed that [Ca2+]c overload induced by Mo originated from ER. Additionally, PLC inhibitor U‐73122 remarkably mitigated the change, and dramatically reduced the number of apoptotic cells, the expression of Bak‐1, Bax, cleaved‐Caspase‐3/Caspase‐3, and notably increased the expression of Bcl‐xL, Bcl‐2, and Bcl‐2/Bax ratio. Overall, the results confirmed that the Ca2+ liberation of ER via PLC/IP3/IP3R axis was the main cause of [Ca2+]c overload, and then stimulated apoptosis in duck renal tubular epithelial cells. [ABSTRACT FROM AUTHOR]

Soybean provides large amounts of protein for human, and the most popular consumption pattern is tofu and soymilk. Recently, the demand of tofu and soymilk is increased, and the breeding of special variety becomes very urgent. To illustrate the genetic basis of these traits, 269 accessions were evaluated under six environments, and 32 associated SNPs were identified on nine chromosomes across multiple environments or conferring diverse traits. Of these SNPs, 16 were demonstrated by BLUP values. Seven adjacent‐SNPs were first identified to associate with tofu and soymilk weights in an 1.02‐Mb region on chromosome 8, which were verified by BLUP‐values. Meanwhile, four neighbouring SNPs in a 0.32‐Mb region on chromosome 12 were first identified to associate with these traits across multiple environments, of which three were detected in BLUP values. Furthermore, some candidate genes, that is, α‐glucan water dikinase Glyma.08G283700 and E3 SUMO‐protein ligase Glyma.12G071300, were screened out with differential expressions between the high‐ and low‐tofu/soymilk‐output accessions. Thus, these associated SNPs and candidate genes provide new insight into the genetic basis of tofu and soymilk processing quality in soybean. [ABSTRACT FROM AUTHOR]

Seed coat cracking (SCC) is a major factor that affects seed appearance quality, pathogen infection, humility absorption and seed storage in soybean. In view of this, a recombinant inbred line (RIL) population and a natural population were genotyped by SoySNP6K and were evaluated for type‐I SCC percentage. Eight QTLs were identified on six chromosomes with phenotypic variation explanations ranging from 3.46% to 34.71% in RIL population. Twenty‐three SNPs associated with cracking percentage were identified on eight chromosomes in natural population. More importantly, the association SNP ss715593768 in natural population was the left marker of qSCC‐C2‐1 in RIL population, which were detected across all of the environments and BLUP values. Two genes, Glyma.06G197300 and Glyma.06G202100, were proposed in this QTL region. These two genes showed differential expressions at seed developmental stages between RIL parents in the seed transcriptome sequencing and quantitative reverse transcription‐polymerase chain reaction (qRT‐PCR) analysis, and also showed differential expressions between two germplasms with different cracking percentage in natural population. Thus, the results provide novel insight into the genetic basis and molecular improvement of SCC in soybean. [ABSTRACT FROM AUTHOR]

Excessive amounts of molybdenum (Mo) and cadmium (Cd) are toxicant, but their combined immunotoxicity are not clearly understood. To estimate united impacts of Mo and Cd on pyroptosis and autophagy by PI3K/AKT axis in duck spleens, Mo or/and Cd subchronic toxicity models of ducks were established by feeding diets with different dosages of Mo or/and Cd. Data show that Mo or/and Cd cause oxidative stress by increasing MDA concentration, and decreasing T‐AOC, CAT, GSH‐Px and T‐SOD activities, restrain PI3K/AKT axis by decreasing PI3K, AKT, p‐AKT expression levels, which evokes pyroptosis and autophagy by elevating IL‐1β, IL‐18 concentrations and NLRP3, Caspase‐1, ASC, GSDME, GSDMA, NEK7, IL‐1β, IL‐18 expression levels, promoting autophagosomes, LC3 puncta, Atg5, LC3A, LC3B, LC3II/LC3I and Beclin‐1 expression levels, and reducing expression levels of P62 and Dynein. Furthermore, the variations of abovementioned indexes are most pronounced in co‐treated group. Overall, results reveal that Mo or/and Cd may evoke pyroptosis and autophagy by PI3K/AKT axis in duck spleens. The association of Mo and Cd exacerbates the changes. [ABSTRACT FROM AUTHOR]

The accumulation of copper (Cu) in the organisms could lead to kidney damage by causing mitochondrial dysfunction. Given that mitochondria are one of the targets of Cu poisoning, this study aimed to investigate the role of mitophagy in Cu‐induced mitochondrial dysfunction in renal tubular epithelial cells to understand the mechanism of Cu nephrotoxicity. Hence, the cells were treated with different concentrations of Cu sulfate (CuSO4) (0, 100, and 200 μM), and mitophagy inhibitor (Cyclosporine A, 0.5 μM) and/or 200 μM CuSO4 in the combination for 12 h. Results showed that Cu caused mitochondrial swelling, vacuoles, and cristae fracture; increased the number of mitochondrial and lysosome fluorescent aggregation points; upregulated the mRNA levels of mitophagy‐associated genes (LC3A, LC3B, P62, BNIP3, NIX, OPTN, NDP52, Cyp D LAMP1, and LAMP2) and protein levels of LC3II/LC3I, BNIP3, and NIX, downregulated the mRNA and protein levels of P62; reduced the mitochondrial membrane potential (MMP), ATP content, mitochondrial respiratory control rate (RCR), mitochondrial respiratory control rate (OPR), and the mRNA and protein levels of PGC‐1α, TOMM20, and Mfn2, but increased the mRNA and protein levels of Drp1. Besides, cotreatment with Cu and CsA dramatically decreased the level of mitophagy, but increased mitochondrial division, further reduced MMP, ATP content, RCR, and OPR, mitochondrial fusion and thereby reduced mitochondrial biogenesis. Taken together, these data indicated that Cu exposure induced BNIP3/NIX‐dependent mitophagy in duck renal tubular epithelial cells, and inhibition of mitophagy aggravated Cu‐induced mitochondrial dysfunction. [ABSTRACT FROM AUTHOR]

High molybdenum (Mo) and cadmium (Cd) are harmful to the body, but pulmonary toxicity induced by Mo and Cd co‐exposure is unknown. To assess the combined impacts of Mo and Cd on fibrosis through M1 polarization in the lung of ducks, 80 healthy 8‐day‐old Shaoxing ducks (Anas platyrhyncha) were randomly assigned to 4 groups and fed with containing unequal doses of Mo or/and Cd diet. Lung tissues were collected on the 16th week. Results indicated that Mo or/and Cd significantly increased their contents in the lungs, and led to trace elements disorder and histological abnormality, and oxidative stress accompanied by promoting contents of H2O2 and MDA and decreasing activities of T‐SOD, GSH‐Px, and CAT, then activated the TLR4/NF‐κB/NLRP3 pathway accompanied by upregulating Caspase‐1, ASC, IL‐18, IL‐1β, TLR4, NF‐κB, and NLRP3 expression levels, and disrupted M1/M2 balance to divert toward M1, which evoked the TGF‐β/Smad2/3‐mediated fibrosis by elevating TGF‐β1, Smad2, Smad3, COL1A1, α‐SMA, and MMP2 expression levels, and decreasing Smad7 and TIMP2 expression levels. The changes of the combined group were most obvious. To sum up, the research demonstrated that Mo or/and Cd may cause macrophages to polarize toward M1 by oxidative stress‐mediated the TLR4/NF‐κB/NLRP3 pathway, then result in fibrosis through the TGF‐β1/Smad2/3 pathway in duck lungs. Mo and Cd may worsen lung damage. [ABSTRACT FROM AUTHOR]

Cadmium (Cd) is detrimental to animals, but nephrotoxic effects of Cd on duck have not been fully elucidated. To evaluate the impacts of Cd on Ca homeostasis and autophagy via PLC‐IP3‐IP3R pathway, primary duck renal tubular epithelial cells were exposed to 2.5 μM and 5.0 μM Cd, and combination of 5.0 μM Cd and 10.0 μM 2‐APB or 0.125 μM U‐73122 for 12 h (U‐73122 pretreated for 1 h). These results evidenced that Cd induced [Ca2+]c overload mainly came from intracellular Ca store. Cd caused [Ca2+]mit and [Ca2+]c overload with [Ca2+]ER decrease, elevated Ca homeostasis related factors (GRP78, GRP94, CRT, CaN, CaMKII, and CaMKKβ) expression, PLC and IP3 activities and IP3R expression, but subcellular Ca2+ redistribution was reversed by 2‐APB. PLC inhibitor U‐73122 dramatically relieved the changes of the above indicators induced by Cd. Additionally, U‐73122 obviously reduced the number of autophagosomes and LC3 accumulation spots, Atg5, LC3A, LC3B mRNA levels and LC3II/LC3I, Beclin‐1 protein levels induced by Cd, and markedly elevated p62 mRNA and protein levels. Overall, the results verified that Cd induced [Ca2+]c overload mainly originated from ER Ca2+ release mediated by PLC‐IP3‐IP3R pathway, then triggered autophagy in duck renal tubular epithelial cells. [ABSTRACT FROM AUTHOR]

Cadmium (Cd) is an environmental pollutant that has an enormous influence on agricultural production, but selenium (Se) can alleviate its toxicity. The present study aimed to illustrate the effects of Se on Cd‐induced heart injury. All 40 rabbits were randomly divided into four groups: control group, Se [0.5 mg kg−1·body weight (BW)] group, Cd (1 mg kg−1·BW) group, and Se + Cd group. After 30 days of feeding, morphological changes, the levels of oxidative stress and myocardial enzyme, the content of cardiac troponin T, programmed cell death (pyroptosis, autophagy and apoptosis), and PI3K/AKT/PTEN transduction capacity were observed. The results showed that Cd destroyed the physiological balance of trace elements and caused myocardial damage, increased the cardiac oxidative damage and led to programmed cell death. Coadministration of Se prominently ameliorated histological lesions and improved cardiac function of hearts in Cd‐induced rabbits. Furthermore, Se exerted detoxification and oxidation resistance, maintained trace element homeostasis, and alleviated the changes of mRNA and protein levels of pyroptosis‐, autophagy‐ and apoptosis‐controlling factors and PI3K/AKT/PTEN signal molecules caused by Cd. In conclusion, Se might protect against Cd‐induced pyroptosis, autophagy and apoptosis by interfering with PI3K/AKT/PTEN signaling in heart. [ABSTRACT FROM AUTHOR]

Summary: Legume–rhizobia symbiosis enables biological nitrogen fixation to improve crop production for sustainable agriculture. Small heat shock proteins (sHSPs) are involved in multiple environmental stresses and plant development processes. However, the role of sHSPs in nodule development in soybean remains largely unknown. In the present study, we identified a nodule‐localized sHSP, called GmHSP17.9, in soybean, which was markedly up‐regulated during nodule development. GmHSP17.9 was specifically expressed in the infected regions of the nodules. GmHSP17.9 overexpression and RNAi in transgenic composite plants and loss of function in CRISPR‐Cas9 gene‐editing mutant plants in soybean resulted in remarkable alterations in nodule number, nodule fresh weight, nitrogenase activity, contents of poly β‐hydroxybutyrate bodies (PHBs), ureide and total nitrogen content, which caused significant changes in plant growth and seed yield. GmHSP17.9 was also found to act as a chaperone for its interacting partner, GmNOD100, a sucrose synthase in soybean nodules which was also preferentially expressed in the infected zone of nodules, similar to GmHSP17.9. Functional analysis of GmNOD100 in composite transgenic plants revealed that GmNOD100 played an essential role in soybean nodulation. The hsp17.9 lines showed markedly more reduced sucrose synthase activity, lower contents of UDP‐glucose and acetyl coenzyme A (acetyl‐CoA), and decreased activity of succinic dehydrogenase (SDH) in the tricarboxylic acid (TCA) cycle in nodules due to the missing interaction with GmNOD100. Our findings reveal an important role and an unprecedented molecular mechanism of sHSPs in nodule development and nitrogen fixation in soybean. [ABSTRACT FROM AUTHOR]

Seed size and shape are important characteristics in soybean breeding, whereas the genetic basis are still unknown, which constrains the improvement of related traits. In view of this, one recombinant inbred line population was assessed for six related traits under four environments. In total, 10 QTLs controlling the related traits were identified, and five were detected across at least two environments, which located on chromosomes 2, 4, 6, 13, and 16 with phenotypic variation explained (PVE) 3.6% to 9.4%. Among them, qSS‐02 and qSS‐16 were identified to control four and five related traits with pleiotropic effects on chromosomes 2 and 16 across three and two environments, respectively. Meanwhile, qSS‐04 was detected to control all of the six related traits on chromosome 4 under four environments with PVEs 4.5% to 9.4%. Furthermore, the candidate genes, that is, Glyma.04G055100 (big grain protein) and Glyma.13G068500 (cytochrome P450), were screened out for their different expressions between population parents at different seed growth and developmental stages. Thus, these results could provide novel insights for the genetic basis of seed size and shape in soybean. [ABSTRACT FROM AUTHOR]

Soybean mosaic virus (SMV) is a serious disease in soybean production, and the cultivation of resistant variety is the irreplaceable strategy to decrease the virus damage. However, the progress of SMV molecular breeding is limited partly due to the diverse types of SMV strains, solely resistance to virus strain of variety and minor genetic effects of QTLs. In the present study, one major pleiotropic additive QTL, qSMV‐D1b, with phenotypic variation explained that 27.04%–54.23% was identified on chromosome 2, and the favourable allele was from the resistant parent "Qihuang30". Meanwhile, the allele analysis of the flanking markers showed that the favourable genotypes presented high resistance to SC3 and SC7 strains with lower disease index, while the unfavourable genotypes presented high sensitivity with higher disease index. Furthermore, six candidate genes, including four novel resistance genes, Glyma.02G121000, Glyma.02G123000, Glyma.02G123200 and Glyma.02G124700 with different expression levels between resistant and sensitive parents were discovered through transcriptome sequencing and confirmed by quantitative real‐time PCR. The resistance genes and the tightly linked molecular markers can be used for SMV breeding in soybean. [ABSTRACT FROM AUTHOR]

Soybean provides irreplaceable protein and oil. Pods and seeds are essential soybean harvested organs. To illustrate the genetic basis of pod‐ and seed‐related traits, a natural population was assessed for eight related traits under four environments. In all, 15 associated SNPs were identified across multiple environments or controlling various traits, and 11 were verified through BLUP. Two SNPs on chromosome 15 were associated with six traits across multiple environments. Two SNPs on chromosome 2 were also associated with six traits under multiple environments. Significant phenotype differences between favourable and unfavourable alleles/haplotypes under four environments were detected. Significant association of pod length SNP and large‐pod phenotype (pod length ≥4.5 cm) was detected. The genetic basis of elite germplasms was analysed, and 'Chuxiu' possessed all of the 15 favourable alleles with best phenotype. Some candidate genes participating in cell wall structural remodelling, gibberellin and ethylene pathways were selected with different expressions in pod developmental stages. These results provided novel insights into genetic basis and molecular markers/candidate genes for soybean fresh pod and seed genetic improvement. [ABSTRACT FROM AUTHOR]

Glyceraldehyde‐3‐phosphate dehydrogenase (GAPDH) is a multifunctional enzyme that plays critical roles in bacterial pathogenesis in some pathogenic bacteria. In this study, the crystal structure of group B streptococcus GAPDH was determined at 1.36 Å resolution. The structure contained an asymmetric mixed holo tetramer, with two NAD ligands bound to two protomers. Further structural analysis identified interesting phosphate ion‐binding sites, which shed light on its catalytic mechanism. [ABSTRACT FROM AUTHOR]

Genetic improvement of fibre quality is one of the main breeding goals for the upland cotton, Gossypium hirsutum, but there are difficulties with precise selection of traits. Therefore, it is important to improve the understanding of the genetic basis of phenotypic variation. In this study, we conducted phenotyping and genetic variation analyses of 719 diverse accessions of upland cotton based on multiple environment tests and a recently developed Cotton 63K Illumina Infinium SNP array and performed a genome-wide association study ( GWAS) of fibre quality traits. A total of 10 511 polymorphic SNPs distributed in 26 chromosomes were screened across the cotton germplasms, and forty-six significant SNPs associated with five fibre quality traits were detected. These significant SNPs were scattered over 15 chromosomes and were involved in 612 unique candidate genes, many related to polysaccharide biosynthesis, signal transduction and protein translocation. Two major haplotypes for fibre length and strength were identified on chromosomes Dt11 and At07. Furthermore, by combining GWAS and transcriptome analysis, we identified 163 and 120 fibre developmental genes related to length and strength, respectively, of which a number of novel genes and 19 promising genes were screened. These results provide new insight into the genetic basis of fibre quality in G. hirsutum and provide candidate SNPs and genes to accelerate the improvement of upland cotton. [ABSTRACT FROM AUTHOR]